QCD Correction to Neutralino Annihilation Process and Dark Matter Density in Supersymmetric Models

We calculate QCD correction to the neutralino annihilation cross section into quark anti-quark final state and discuss its implications to the calculation of neutralino relic density. We see that the QCD correction enhances the pair-annihilation cross section by O(10 %) when final-state quarks are non-relativistic. Consequently, when the lightest neutralinos dominantly annihilate into a t\bar{t} pair, the relic density of the lightest neutralino is significantly affected by the QCD correction, in particular when the lightest-neutralino mass is close to the top-quark mass.Comment: 19 pages, 5 figure

Measurement of hepatitis B virus core-related antigen is valuable for identifying patients who are at low risk of lamivudine resistance

ArticleLIVER INTERNATIONAL. 26(1): 90-96 (2006)journal articl

Immunological and molecular epidemiological characteristics of acute and fulminant viral hepatitis A

<p>Abstract</p> <p>Background</p> <p>Hepatitis A virus is an infection of liver; it is hyperendemic in vast areas of the world including India. In most cases it causes an acute self limited illness but rarely fulminant. There is growing concern about change in pattern from asymptomatic childhood infection to an increased incidence of symptomatic disease in the adult population.</p> <p>Objective</p> <p>In-depth analysis of immunological, viral quantification and genotype of acute and fulminant hepatitis A virus.</p> <p>Methods</p> <p>Serum samples obtained from 1009 cases of suspected acute viral hepatitis was employed for different biochemical and serological examination. RNA was extracted from blood serum, reverse transcribed into cDNA and amplified using nested PCR for viral quantification, sequencing and genotyping. Immunological cell count from freshly collected whole blood was carried out by fluorescence activated cell sorter.</p> <p>Results</p> <p>Fulminant hepatitis A was mostly detected with other hepatic viruses. CD8⁺T cells count increases in fulminant hepatitis to a significantly high level (P = 0.005) compared to normal healthy control. The immunological helper/suppressor (CD4⁺/CD8⁺) ratio of fulminant hepatitis was significantly lower compared to acute cases. The serologically positive patients were confirmed by RT-PCR and total of 72 (69.2%) were quantified and sequenced. The average quantitative viral load of fulminant cases was significantly higher (<it>P </it>< 0.05). There was similar genotypic distribution in both acute and fulminant category, with predominance of genotype IIIA (70%) compared to IA (30%).</p> <p>Conclusions</p> <p>Immunological factors in combination with viral load defines the severity of the fulminant hepatitis A. Phylogenetic analysis of acute and fulminant hepatitis A confirmed genotypes IIIA as predominant against IA with no preference of disease severity.</p

Cellular immunity in children with successful immunoprophylactic treatment for mother-to-child transmission of hepatitis B virus

Background: The administration of hepatitis B immunoglobulin followed by hepatitis B vaccine can result in a protective efficacy of almost 90% in mother-to-child transmission of hepatitis B virus (HBV). However, little is known about immunity against HBV infection in children after immunoprophylactic treatment. We tried to assess the association between T-cell responses and viremia in children after successful prophylactic treatment. Methods: Thirteen children and their 8 HBV carrier mothers (8 families), who were positive for human leukocyte antigen (HLA)-A24, were enrolled in this study. All of the 13 children received immunoprophylactic treatment and became negative for hepatitis B surface antigen (HBsAg) after birth. HBV-specific cytotoxic T lymphocyte (CTL) responses were evaluated using IFNγ - enzyme-linked immunosorbent spot (ELISPOT) and major histocompatibility complex class I peptide pentamer assays. Serum HBV DNA was measured by real-time PCR. Results: Significant HBV-specific T-cell responses were detected in 2 (15%) of the 13 children by ELISPOT. However, the frequency of HLA-A24-HBV-specific CTLs was very low in both HBV carrier mothers and children using pentamers. Of the 13 children, 4 (31%) were positive for serum HBV DNA. However, the levels of serum HBV DNA were 100 copies/ml or less. One of the 2 children in whom significant HBV-specific CTL responses were detectable was positive for serum HBV DNA. Conclusions: HBV core and polymerase-specific T-cell responses were detected and a low-dose viremia was observed in children after successful immunoprophylaxis treatment. Although the presence of viremia was not related to HBV-specific T-cell responses, CTLs might play a role in the control of HBV infection in children born to HBsAg-positive mothers after immunoprophylactic treatment. </p

Mass spectrum of primordial black holes from inflationary perturbation in the Randall-Sundrum braneworld: a limit on blue spectra

The mass spectrum of the primordial black holes formed by density perturbation in the radiation-dominated era of the Randall-Sundrum type-2 cosmology is given. The spectrum coincides with standard four-dimensional one on large scales but the deviation is apparent on smaller scales. The mass spectrum is initially softer than standard four-dimensional one, while after accretion during the earliest era it becomes harder than that. We also show expected extragalactic diffuse photon background spectra varying the initial perturbation power-law power spectrum and give constraints on the blue spectra and/or the reheating temperature. The most recent observations on the small scale density perturbation from WMAP, SDSS and Lyman-\alpha Forest are used. What we get are interpreted as constraints on the smaller scale inflation on the brane connected to the larger one at the scale of Lyman-\alpha Forest. If we set the bulk curvature radius to be 0.1 mm and assume the reheating temperature is higher than 10^6 GeV, the scalar spectral index from the smaller scale inflation is constrained to be n \lesssim 1.3. Typically, the constraints are tighter than standard four-dimensional one, which is also revised by us using the most recent observations.Comment: 19 pages, 6 figures; typos corrected, references added, published in JCA

Defending the genome from the enemy within:mechanisms of retrotransposon suppression in the mouse germline

The viability of any species requires that the genome is kept stable as it is transmitted from generation to generation by the germ cells. One of the challenges to transgenerational genome stability is the potential mutagenic activity of transposable genetic elements, particularly retrotransposons. There are many different types of retrotransposon in mammalian genomes, and these target different points in germline development to amplify and integrate into new genomic locations. Germ cells, and their pluripotent developmental precursors, have evolved a variety of genome defence mechanisms that suppress retrotransposon activity and maintain genome stability across the generations. Here, we review recent advances in understanding how retrotransposon activity is suppressed in the mammalian germline, how genes involved in germline genome defence mechanisms are regulated, and the consequences of mutating these genome defence genes for the developing germline

A comparison of hepatitis B viral markers of patients in different clinical stages of chronic infection

Hepatitis B viral markers may be useful for predicting outcomes such as liver-related deaths or development of hepatocellular carcinoma. We determined the frequency of these markers in different clinical stages of chronic hepatitis B infection. We compared baseline hepatitis B viral markers in 317 patients who were enrolled in a prospective study and identified the frequency of these tests in immune-tolerant (IT) patients, in inactive carriers , and in patients with either hepatitis B e antigen ( HBeAg)- positive or HBeAg-negative chronic hepatitis or cirrhosis. IT patients were youngest (median age 27 years) and HBeAg- negative patients with cirrhosis were oldest (median age 58 years) (p = 0.03 to < 0.0001). The male to female ratio was similar both in IT patients and in inactive carriers, but there was a male preponderance both in patients with chronic hepatitis and in patients with cirrhosis (p < 0.0001). The A1896 precore mutants were most prevalent in inactive carriers (36.4%) and HBeAg- negative patients with chronic hepatitis (38.8%; p < 0.0001), and the T 1762/A1764 basal core promoter mutants were most often detected in HBeAg- negative patients with cirrhosis (65.1%; p = 0.02). Genotype A was detected only in 5.3% of IT patients, and genotype B was least often detected in both HBeAg-Positive patients with chronic hepatitis and cirrhosis (p = 0.03). The hepatitis B viral DNA levels were lowest in inactive carriers (2.69 log(10) IU/mL) and highest in IT patients (6. 80 log(10) IU/mL; p = 0.02 to < 0.0001). At follow-up, HBeAg-positive and HBeAg-negative patients with cirrhosis accounted for 57 of 64 (89.1%) liver-related deaths (p < 0. 0001). Differences in baseline hepatitis B viral markers were detected in patients in various clinical stages of hepatitis B virus infection. HBeAg-positive and HBeAg- negative patients with cirrhosis accounted for the majority of the liver-related fatalities

Molecular characterization of hepatitis B virus X gene in chronic hepatitis B patients

BACKGROUND: HBV-X protein is associated with the pathogenesis of HBV related diseases, specially in hepatocellular carcinomas of chronic patients. Genetic variability of the X gene includes genotypic specific variations and mutations emerging during chronic infection. Its coding sequence overlaps important regions for virus replication, including the basal core promoter. Differences in the X gene may have implications in biological functions of the protein and thus, affect the evolution of the disease. There are controversial results about the consequences of mutations in this region and their relationship with pathogenesis. The purpose of this work was to describe the diversity of HBV-X gene in chronic hepatitis patients infected with different genotypes, according to liver disease. METHODS: HBV-X gene was sequenced from chronic hepatitis B patient samples, analyzed by phylogeny and genotyped. Nucleotide and aminoacid diversity was determined calculating intragenetic distances. Mutations at 127, 130 and 131 aminoacids were considered in relation to liver disease. RESULTS: The most prevalent genotype detected in this cohort was F (F1 and F4), followed by D and A. Most of the samples corresponding to genotypes A and F1 were HBeAg(+) and for genotypes D and F4, HBeAg(−) samples were represented in a higher percentage. Intragenetic distance values were higher in HBeAg(−) than in positive samples for all genotypes, and lower in overlapped regions, compared to single codification ones. Nucleotide and aminoacid diversities were higher in HBeAg(−), than in HBeAg(+) samples. CONCLUSIONS: Independently of the infecting genotypes, mutations at any of 127, 130 and/or 131 aminoacid positions and HBeAg(−) status were associated with mild liver disease in this cohort

Trends in prevalence of hepatitis B virus infection among Albanian blood donors, 1999-2009

<p>Abstract</p> <p>Background</p> <p>Hepatitis B virus (HBV) was among the first virus known to be transmitted by blood and blood productions. The objective of this study is to determine the trend of hepatitis B virus in blood donors.</p> <p>Materials and methods</p> <p>In this study 79274 blood donors were retrospectively evaluated for HBsAg. The donors were selected using personal questionnaire, physical examination and testing blood before donation. Blood banks records are used as source of information. The blood donors samples were analyzed for the presence of hepatitis B surface antigen (HBsAg) by commercial available kits ELISA method, third generation (from Abbott laboratory, Germany). A sample was considered as HBsAg positive when found twice repeatedly reactive. Reactive samples were not confirmed with addition tests.</p> <p>Results</p> <p>In the evaluation data, we found out that from 79274 of the total healthy blood donors, 15983 were voluntary donors, 52876 were family replacement donors and 10424 commercial blood donors. The prevalence of HBsAg in blood donors was 7.9%. It was increased steadily from 5.9% in 1999 to 9.1% in 2006 and decreased in 7.9% in 2009. According to blood donors status the HBsAg prevalence was 10.5% in commercial blood donors, 8.1% in voluntary donors and 8.6% in family replacement donors. The prevalence of anti-HBc in blood donors was 59.1%.</p> <p>Conclusion</p> <p>The prevalence of HBsAg was lower in voluntary non remunerate blood donors than commercial donors and family replacement blood donors. In FDs the prevalence was higher than VDs but lower than CDs. So, it is important to encourage the voluntary blood donors to become regularly blood donors.</p